How does mushroom poisoning occur?

Mushroom poisoning is caused by the consumption of raw or cooked
fruiting bodies (mushrooms, toadstools) of a number of species of
higher fungi. The term toadstool (from the German Todesstuhl,
death's stool) is commonly given to poisonous mushrooms. However,
for individuals who are not experts in mushroom identification,
there are generally no easily recognizable differences between
poisonous and nonpoisonous species. Old wives' tales
notwithstanding, there is no general rule of thumb for
distinguishing edible mushrooms and poisonous toadstools. The
toxins involved in mushroom poisoning are produced naturally by the
fungi themselves, and each individual specimen of a toxic species
should be considered equally poisonous.

Most mushrooms that cause human poisoning cannot be made
nontoxic by cooking, canning, freezing, or any other means of
processing. Thus, the only way to avoid poisoning is to avoid
consumption of the toxic species. Poisonings in the United States
occur most commonly when:

Hunters of wild mushrooms (especially novices) misidentify and
consume a toxic species

Recent immigrants collect and consume a poisonous American
species that closely resembles an edible wild mushroom from their
native land

Mushrooms that contain psychoactive compounds are intentionally
consumed by persons who desire these effects.

What are the characteristics of mushroom poisoning?

Mushroom poisonings are generally acute and are manifested by a
variety of symptoms and prognoses, depending on the amount and
species consumed. Because positive identification of the mushrooms
is often difficult or impossible, mushroom poisonings are generally
categorized by their physiological effects. There are four
categories of mushroom toxins:

Protoplasmic poisons
(poisons that result in generalized
destruction of cells, followed by organ failure)

Disulfiram-like toxins
(Mushrooms in this last category
are generally nontoxic and produce no symptoms unless alcohol is
consumed within 72 hours after eating them, in which case a
short-lived acute toxic syndrome is produced).

How is mushroom poisoning diagnosed?

A clinical testing procedure is currently available only for the
most serious types of mushroom toxins, the amanitins. The
commercially available method can detect the toxin in urine and
plasma. Unfortunately, it requires a 2-hour incubation period, and
this is an excruciating delay in a type of poisoning which the
clinician generally does not see until a day or two has passed.
Positive botanical identification of the mushroom species consumed
remains the only means of unequivocally determining the particular
type of intoxication involved. It is still vitally important to
obtain such accurate identification as quickly as possible. Cases
involving ingestion of more than one toxic species in which one set
of symptoms masks or mimics another set are among many reasons for
needing this information.

Unfortunately, a number of factors (not discussed here) often
make identification of the causative mushroom impossible. In such
cases, diagnosis must be based on symptoms alone. In order to rule
out other types of food poisoning and to conclude that the
mushrooms eaten were the cause of the poisoning, it must be
established that everyone who ate the suspect mushrooms became ill
and that no one who did not eat the mushrooms became ill. Wild
mushrooms eaten raw, cooked, or processed should always be regarded
as prime suspects. The importance of rapid diagnosis is obvious:
victims who are hospitalized and given aggressive support
therapy almost immediately after ingestion have a mortality rate of
only 10%, whereas those admitted 60 or more hours after ingestion
have a 50-90% mortality rate.

Which mushrooms are associated with mushroom poisoning?

Mushroom poisonings are almost always caused by ingestion of
wild mushrooms that have been collected by nonspecialists (although
specialists have also been poisoned). Most cases occur when toxic
species are confused with edible species, and a useful question to
ask of the victims or their mushroom-picking benefactors is the
identity of the mushroom they thought they were picking. In the
absence of a well- preserved specimen, the answer to this question
could narrow the possible suspects considerably.

Intoxication has also occurred when reliance was placed on some
folk method of distinguishing poisonous and safe species. Outbreaks
have occurred after ingestion of:

Fresh, raw mushrooms

Stir-fried mushrooms

Home-canned mushrooms

Mushrooms cooked in tomato sauce (which rendered the sauce
itself toxic, even when no mushrooms were consumed)

Mushrooms that were blanched and frozen at home

Cases of poisoning by home-canned and frozen mushrooms are
especially insidious. A single outbreak may easily become a
multiple outbreak when the preserved toadstools are carried to
another location and consumed at another time.

Specific cases of mistaken mushroom identity appears frequently.
The Early False Morel
Gyromitra esculenta
is easily confused
with the true Morel
Morchella esculenta
, and poisonings have
occurred after consumption of fresh or cooked
Gyromitra
.
Gyromitra
poisonings have also occurred after ingestion of
commercially available "morels" contaminated with
G.
esculenta
. The commercial sources for these fungi (which have
not yet been successfully cultivated on a large scale) are field
collection of wild morels by semiprofessionals. Cultivated
commercial mushrooms of whatever species are almost never
implicated in poisoning outbreaks unless there are associated
problems such as improper canning (which lead to bacterial food
poisoning).

Producers of mild gastroenteritis are too numerous to list here,
but include members of many of the most abundant genera, including:
Agaricus
,
Boletus
,
Lactarius
,
Russula
,
Tricholoma
,
Coprinus
,
Pluteus
, and others. The
Inky Cap Mushroom
(
Coprinus atrimentarius
) is
considered both edible and delicious, and only the unwary who
consume alcohol after eating this mushroom need be concerned. Some
other members of the genus
Coprinus
(
Shaggy Mane
,
C. comatus
;
Glistening Inky Cap
,
C. micaceus
,
and others) and some of the larger members of the
Lepiota
family such as the
Parasol Mushroom
(Leucocoprinus procera)
do not contain coprine and do not cause this effect.

The potentially deadly
Sorrel Webcap Mushroom
(
Cortinarius orellanus
) is not easily distinguished from
nonpoisonous webcaps belonging to the same distinctive genus, and
all should be avoided. Most of the psychotropic mushrooms
(
Inocybe
spp.,
Conocybe
spp.,
Paneolus
spp.,
Pluteus
spp.) are in general appearance small, brown, and
leathery (the so-called "Little Brown Mushrooms" or LBMs) and
relatively unattractive from a culinary standpoint. The
Sweat
Mushroom
(
Clitocybe dealbata
) and the
Smoothcap
Mushroom
(
Psilocybe cubensis
) are small, white, and
leathery. These small, unattractive mushrooms are distinctive,
fairly unappetizing, and not easily confused with the fleshier
fungi normally considered edible. Intoxications associated with
them are less likely to be accidental, although both
C.
dealbata
and
Paneolus foenisicii
have been found growing
in the same fairy ring area as the edible (and choice)
Fairy
Ring Mushroom
(
Marasmius oreades
) and the
Honey
Mushroom
(
Armillariella mellea
). They have been consumed
when the picker has not carefully examined every mushroom picked
from the ring.

Psychotropic mushrooms, which are larger and therefore more
easily confused with edible mushrooms, include the
Showy
Flamecap
or
Big Laughing Mushroom
(Gymnopilus
spectabilis), which has been mistaken for
Chanterelles
(
Cantharellus
spp.) and for
Gymnopilus ventricosus
found growing on wood of conifers in western North America. The
Fly Agaric
(
Amanita muscaria)
and
Panthercap
(
Amanita pantherina
) mushrooms are large, fleshy, and
colorful. Yellowish cap colors on some varieties of the Fly Agaric
and the Panthercap are similar to the edible
Caesar's
Mushroom
(
Amanita caesarea
), which is considered a
delicacy in Italy.

Another edible yellow capped mushroom occasionally confused with
yellow
A. muscaria
and
A. pantherina
varieties are
the
Yellow Blusher
(
Amanita flavorubens
). Orange to
yellow-orange
A. muscaria
and
A. pantherina
may also
be confused with the
Blusher
(
Amanita rubescens
) and
the
Honey Mushroom
(
Armillariella mellea
). White to
pale forms of
A. muscaria
may be confused with edible field
mushrooms (
Agaricus
spp.). Young (button stage) specimens of
A. muscaria h
ave also been confused with
puffballs
.

How often do mushroom poisonings occur?

Accurate figures on the relative frequency of mushroom
poisonings are difficult to obtain. The number of unreported cases
is, of course, unknown. Cases are sporadic and large outbreaks are
rare. Poisonings tend to be grouped in the spring and fall when
most mushroom species are at the height of their fruiting stage.
While the actual incidence appears to be very low, the potential
exists for grave problems. Poisonous mushrooms are not limited in
distribution as are other poisonous organisms (such as
d
inoflagellates
). Intoxications may occur at any time and
place, with dangerous species occurring in habitats ranging from
urban lawns to deep woods. As Americans become more adventurous in
their mushroom collection and consumption, poisonings are likely to
increase.

What are the symptoms and complications of mushroom
poisoning?

The normal course of the disease varies with the dose and the
mushroom species eaten. Each poisonous species contains one or more
toxic compounds which are unique to few other species. Therefore,
cases of mushroom poisonings generally do not resembles each other
unless they are caused by the same or very closely related mushroom
species. Almost all mushroom poisonings may be grouped in one of
the categories outlined above.

PROTOPLASMIC POISONS

Amatoxins:

Several mushroom species, including the
Death Cap
or
Destroying Angel
(
Amanita phalloides
,
A.
virosa
), the
Fool's Mushroom
(
A. verna
) and
several of their relatives, along with the
Autumn Skullcap
(
Galerina autumnalis
) and some of its relatives, produce
amanitins. Poisoning by the amanitins is characterized by a long
latent period (6-48 hours, average 6-15 hours) during which the
patient shows no symptoms. Symptoms appear at the end of the latent
period in the form of::

Sudden, severe seizures of abdominal pain

Persistent vomiting and watery diarrhea

Extreme thirst

Lack of urine production.

If this early phase is survived, the patient may appear to
recover for a short time, but this period will generally be
followed by a rapid and severe loss of strength, prostration, and
pain-caused restlessness. Death in 50-90% of the cases from
progressive and irreversible liver, kidney, cardiac, and skeletal
muscle damage may follow within 48 hours (large dose).The disease
more typically lasts 6 to 8 days in adults and 4 to 6 days in
children. Two or three days after the onset of the later phase,
jaundice, cyanosis, and coldness of the skin occur. Death usually
follows a period of coma and occasionally convulsions. If recovery
occurs, it generally requires at least a month and is accompanied
by enlargement of the liver. Autopsy will usually reveal fatty
degeneration and necrosis of the liver and kidney.

Hydrazines:

Certain species of
False Morel
(
Gyromitra
esculenta
and
G. gigas
) contain the protoplasmic poison
gyromitrin. Poisoning by this toxin superficially resembles Amanita
poisoning but is less severe. There is generally a latent period of
6 - 10 hours after ingestion during which no symptoms are evident,
followed by sudden onset of:

Abdominal discomfort (a feeling of fullness)

Severe headache

Vomiting

Sometimes diarrhea

The toxin affects primarily the liver, but there are additional
disturbances to blood cells and the central nervous system. The
mortality rate is relatively low (2-4%). Poisonings with symptoms
almost identical to those produced by
Gyromitra
have also
been reported after ingestion of the
Early False Morel
(
Verpa bohemica
). The toxin is presumed to be related to
gyromitrin but has not yet been identified.

Orellanine:

The final type of protoplasmic poisoning is caused by the
Sorrel WebcapMushroom
(
Cortinarius orellanus
)
and some of its relatives. This mushroom causes a type of poisoning
characterized by an extremely long symptom-free period of 3 to 14
days. An intense, burning thirst (polydipsia) and excessive
urination (polyuria) are the first symptoms. This may be followed
by nausea, headache, muscular pains, chills, spasms, and loss of
consciousness. In severe cases, severe renal tubular necrosis and
kidney failure may result in death (15%) several weeks after the
poisoning. Fatty degeneration of the liver and severe inflammatory
changes in the intestine accompany the renal damage, and recovery
in less severe cases may require several months.

NEUROTOXINS

Poisonings by mushrooms that cause neurological problems may be
divided into three groups, based on the type of symptoms produced,
and named for the substances responsible for these symptoms.

Muscarine poisoning:

Ingestion of any number of
Inocybe
or
Clitocybe
species (e.g.,
Inocybe geophylla
,
Clitocybe dealbata
)
results in an illness characterized primarily by profuse sweating.
This effect is caused by the presence in these mushrooms of high
levels (3- 4%) of muscarine. Muscarine poisoning is characterized
by increased salivation, perspiration, and lacrimation within 15 to
30 minutes after ingestion of the mushroom. With large doses, these
symptoms may be followed by abdominal pain, severe nausea,
diarrhea, blurred vision, and labored breathing. Intoxication
generally subsides within 2 hours. Deaths are rare, but may result
from cardiac or respiratory failure in severe cases.

Ibotenic acid/Muscimol poisoning:

The
Fly Agaric
(
Amanita muscaria
) and
Panthercap
(
Amanita pantherina
) mushrooms both
produce ibotenic acid and muscimol. Both substances produce the
same effects, but muscimol is approximately 5 times more potent
than ibotenic acid. Symptoms of poisoning generally occur within 1
- 2 hours after ingestion of the mushrooms. An initial abdominal
discomfort may be present or absent, but the chief symptoms are
drowsiness and dizziness (sometimes accompanied by sleep), followed
by a period of hyperactivity, excitability, illusions, and
delirium. Periods of drowsiness may alternate with periods of
excitement, but symptoms generally fade within a few hours.
Fatalities rarely occur in adults, but in children, accidental
consumption of large quantities of these mushrooms may cause
convulsions, coma, and other neurologic problems for up to 12
hours.

Psilocybin poisoning:

A number of mushrooms belonging to the genera
Psilocybe
,
Panaeolus
,
Copelandia
,
Gymnopilus
,
Conocybe
, and
Pluteus
, when ingested, produce a
syndrome similar to alcohol intoxication (sometimes accompanied by
hallucinations). Onset of symptoms is usually rapid and the effects
generally subside within 2 hours. Poisonings by these mushrooms are
rarely fatal in adults and may be distinguished from ibotenic acid
poisoning by the absence of drowsiness or coma. The most severe
cases of psilocybin poisoning occur in small children, where large
doses may cause the hallucinations accompanied by fever,
convulsions, coma, and death. These mushrooms are generally small,
brown, nondescript, and not particularly fleshy; they are seldom
mistaken for food fungi by innocent hunters of wild mushrooms.
Poisonings caused by intentional ingestion of these mushrooms by
people with no legitimate religious justification must be handled
with care, since the only cases likely to be seen by the physician
are overdoses or intoxications caused by a combination of the
mushroom and some added psychotropic substance (such as PCP).

GASTROINTESTINAL IRRITANTS

Numerous mushrooms, including the
Green Gill
(
Chlorophyllum molybdites
),
Gray Pinkgill
(
Entoloma lividum
),
Tigertop
(
Tricholoma
pardinum
),
Jack O'Lantern
(
Omphalotus illudens
),
Naked Brimcap
(
Paxillus involutus
),
Sickener
(
Russula emetica
),
Early False Morel
(
Verpa
bohemica
),
Horse Mushroom
(
Agaricus arvensis
) and
Pepper bolete
(
Boletus piperatus
), contain toxins
that can cause gastrointestinal distress, including but not limited
to nausea, vomiting, diarrhea, and abdominal cramps. In many ways
these symptoms are similar to those caused by the deadly
protoplasmic poisons. The chief and diagnostic difference is that
poisonings caused by these mushrooms have a rapid onset, rather
than the delayed onset seen in protoplasmic poisonings. Some
mushrooms (including the first five species mentioned above) may
cause vomiting and/or diarrhea which lasts for several days.
Fatalities caused by these mushrooms are relatively rare and are
associated with dehydration and electrolyte imbalances caused by
diarrhea and vomiting, especially in debilitated, very young, or
very old patients. Replacement of fluids and other appropriate
supportive therapy will prevent death in these cases. The chemistry
of the toxins responsible for this type of poisoning is virtually
unknown, but may be related to the presence in some mushrooms of
unusual sugars, amino acids, peptides, resins, and other
compounds.

DISULFIRAM-LIKE POISONING

The
Inky Cap Mushroom
(
Coprinus atramentarius
) is
most commonly responsible for this poisoning, although a few other
species have also been implicated. A complicating factor in this
type of intoxication is that this species is generally considered
edible (i.e.,
no illness results when eaten in the absence of
alcoholic beverages
). Consumption of alcoholic beverages within
72 hours after eating it will cause headache, nausea and vomiting,
flushing, and cardiovascular disturbances that last for 2 - 3
hours.

MISCELLANEOUS POISONINGS

Young fruiting bodies of the sulfur shelf fungus
Laetiporus
sulphureus
are considered edible. However, ingestion of this
shelf fungus has caused digestive upset and other symptoms in
adults and visual hallucinations and ataxia in a child.

Who is susceptible to mushroom poisoning?

All humans are susceptible to mushroom toxins. The poisonous
species are found everywhere, and geographical restrictions on
types of poisoning that may occur in one location do not exist
(except for some of the hallucinogenic LBMs, which occur primarily
in the American southwest and southeast). Individual specimens of
poisonous mushrooms are also characterized by individual variations
in toxin content based on genetics, geographic location, and
growing conditions. Intoxications may thus be more or less serious,
depending not on the number of mushrooms consumed, but on the dose
of toxin delivered. In addition, although most cases of poisoning
by higher plants occur in children, toxic mushrooms are consumed
most often by adults. Occasional accidental mushroom poisonings of
children and pets have been reported, but adults are more likely to
actively search for and consume wild mushrooms for culinary
purposes. Children are more seriously affected by the normally
nonlethal toxins than are adults and are more likely to suffer very
serious consequences from ingestion of relatively smaller doses.
Adults who consume mushrooms are also more likely to recall what
was eaten and when, and are able to describe their symptoms more
accurately than are children. Very old, very young, and debilitated
persons of both sexes are more likely to become seriously ill from
all types of mushroom poisoning, even those types which are
generally considered to be mild.

Many idiosyncratic adverse reactions to mushrooms have been
reported. Some mushrooms cause certain people to become violently
ill, while not affecting others who consumed part of the same
mushroom cap. Factors such as age, sex, and general health of the
consumer do not seem to be reliable predictors of these reactions,
and they have been attributed to allergic or hypersensitivity
reactions and to inherited inability of the unfortunate victim to
metabolize certain unusual fungal constituents (such as the
uncommon sugar, trehalose). These reactions are probably not true
poisonings as the general population does not seem to be
affected.

Source:

Food and Drug
Administration

Please be aware that this information is provided to supplement the care
provided by your physician. It is neither intended nor implied to be a
substitute for professional medical advice. CALL YOUR HEALTHCARE PROVIDER
IMMEDIATELY IF YOU THINK YOU MAY HAVE A MEDICAL EMERGENCY. Always seek the
advice of your physician or other qualified health provider prior to
starting any new treatment or with any questions you may have regarding a
medical condition.